eMedicine Specialties > Pediatrics: General Medicine > Pulmonology
Hypersensitivity Pneumonitis
Updated: Apr 14, 2008
Introduction
Background
Hypersensitivity pneumonitis (HP) refers to a group of disorders caused by a nonatopic immunologic response to an inhaled agent. In its acute or subacute form, HP may be a cause of recurrent pneumonitis. In its chronic form, HP may insidiously lead to pulmonary fibrosis and emphysema. Severe acute or subacute flares can be life threatening,1 and recurrent or chronic disease can lead to permanent, severe lung damage.2 Although rare, fatal cases of chronic HP have been reported in children.3
Hypersensitivity pneumonitides are classically considered occupational illnesses and have colorful names reflecting the associated occupation. Some of these illnesses and their associated causes include the following:4
- Farm worker's lung - Thermophilic actinomycetes and other pathogens
- Winemaker's lung - Botrytis cinerea
- Coffee worker's lung - Coffee bean dust
- Lifeguard's lung - Aerosolized endotoxin
- Poultry worker's lung - Avian antigens
- Laboratory worker's lung - Rodent antigens
- Miller's lung - Wheat weevil
- Woodworker's lung - Penicillium chrysogenum
- Detergent worker's lung - Bacillus subtilis
- Epoxy-resin lung - Phthalic anhydride
Pathophysiology
Numerous organic and inorganic antigens can cause HP. To cause pneumonitis, the antigen must penetrate into the small airways; therefore, its size must be within the respirable range (smaller than 5 μm). Implicated antigens include avian (bird) antigens, mammalian proteins, fungi and fungal spores, bacterial antigens, and small-molecular-weight chemicals.5 See Causes.
Immune responses
The immunopathogenesis of HP has not been well characterized. An exuberant production of antibody (especially immunoglobulin G [IgG]) against the offending antigen is frequently identified; however, the precipitating antibody alone is not sufficient to cause HP. A key role for T-cell mediated responses is suggested by the observations of CD8+ cytotoxic lymphocyte proliferation6 and greater percentages of natural killer T (NKT) cells in bronchoalveolar lavage fluid (BALF).7
Various cytokines have been identified in acute hypersensitivity pneumonitides, but their role is poorly understood; most research has focused on animal models, in vitro systems, and clinical observations. Interleukin (IL)-8 (a chemoattractant of neutrophils) is released by a cell line with properties of alveolar lung cells when stimulated by thermophilic bacteria.8 High levels of IL-8 are released by alveolar macrophages in patients with acute HP.9 Levels of tumor necrosis factor (TNF)-α (a proinflammatory cytokine produced by macrophages) became elevated in patients with acute farmer’s lung after an antigen challenge but were not elevated in unaffected farmers after antigen challenge.10
An important role for interferon-γ (a cytokine important in Th1 response) is suggested by the observation that interferon-γ knockout mice lack granulomatous inflammation in response to stimulation by thermophilic bacteria, whereas granulomatous inflammation develops in both knockout mice given interferon-γ replacement and wild-type mice.11
Genetics
Familial clustering of cases suggests a genetic predisposition, but a clear genetic locus has not yet been identified. Likewise, associations with different human leukocyte antigen (HLA) phenotypes have been suggested, but no clear or consistent pattern has emerged.12,13,14
Viral infections
Viral infections may play a role in triggering HP flares. Research in an animal model suggests that viral infection can augment inflammatory responses in HP.15 This is supported by the finding of respiratory viruses in the BALF of 9 of 13 patients during acute exacerbations of farmer’s lung.16
Frequency
The true prevalence of HP is unknown. Relatively few cases have been described in the pediatric literature.
United States
The frequency in children is unknown.
International
Acute HP in children is more common in areas where pigeon racing and pigeon breeding are popular. Chronic disease is more common in areas where caged birds are typical house pets.
Mortality/Morbidity
Mortality due to HP in childhood is uncommon; however, a fatal case has been reported.3 Significant morbidity can result if the child is not removed from the causative environment.
Severe pulmonary fibrosis with honeycombing and spontaneous pneumothorax (end-stage lung disease) as a consequence of chronic HP has been described in an adolescent.2
In adults, chronic HP with pulmonary fibrosis and honeycombing is associated with high mortality rates.17
Age
See Mortality/Morbidity.
Clinical
History
A comprehensive environmental history and high index of suspicion are critical for diagnosis. Hypersensitivity pneumonitis (HP) should be considered in patients with chronic or recurrent cough, shortness of breath, or a history of recurrent acute respiratory symptoms without definite infectious triggers.
Inquire about specific exposures; the patient may not volunteer them. Because bird fancier’s lung is the most common HP in children, a specific inquiry must be made about bird exposure. Contact may not necessarily be in the home and may not be obvious. Exposures in or near the home, at school, as a part of hobbies, at the place of employment, or anywhere else the child spends time must be explored. Repeated questioning, home inspection, and/or inspection of sites where the child spends time may be needed to identify the causative antigen.
Clues that strongly suggest the diagnosis of HP are as follows:18
- History of recurrent pneumonia, particularly with regularity or a pattern
- Other people at home or school who have similar symptoms
- Development of respiratory symptoms after the patient moves to a new home or new school
- Improvement of symptoms when the patient is away from home or school for an extended period
- Contact with birds
- Water damage to the patient's home or school facility
- Use of a hot tub, sauna, or swimming pool
Manifestations of HP are classified as acute, subacute, or chronic. These classifications should be considered as points along a spectrum of illness rather than clearly delineated, discrete types of illness.19 In patients with acute disease, a temporal relation between the respiratory symptoms and antigenic exposure can usually be identified. In cases of subacute or chronic exposure, the association between antigenic exposure and development of disease may not be obvious.
HP seems to be least common among active smokers of tobacco products. This relative infrequency might result from suppression of alveolar macrophage function.20,21,22 However, a chart review of an outbreak of HP among metalworkers suggested that low disease rates among tobacco smokers may reflect a high proportion of false-negative results instead of a truly low rate of disease.23 Another study suggests that HP may be most insidious and is most often associated with low survival rates when it occurs in smokers.24
Physical
Acute HP is characterized by the abrupt onset (4-6 h after exposure) of fever, chills, malaise, nausea, dry cough, chest tightness, and dyspnea. Physical examination may reveal tachypnea and fine crackles localized to the lung bases; wheezing is unusual. The presentation is easily confused with that of an infectious pneumonia. Removal from exposure usually results in resolution of symptoms within hours to days.
Subacute HP is characterized by the gradual development of productive cough, dyspnea, fatigue, anorexia, weight loss, and low-grade fever. Physical examination and chest auscultation may reveal tachypnea and diffuse crackles. In patients with severe disease, cyanosis may be present.1 Resolution of disease may take weeks to months after removal from exposure.
Chronic HP may be difficult to diagnose in its early stages. A chronic cough with a normal physical exam may be the first presentation. Over time, the disease may progress to dyspnea, fatigue, weight loss, and exercise intolerance. Auscultation of the chest may reveal crackles. An “inspiratory squawk” or “chirping rales” have been described.25,26 Digital clubbing may be seen in the advanced stages of the disease.
Causes
Types and causes of hypersensitivity pneumonitis in children
A wide spectrum of respirable antigens can trigger HP, including avian antigens, rodent antigens, fungi, bacteria, and low molecular weight chemicals. Fungal spores can be present wherever sufficient humidity is present; for example, in piles of moldy hay (farmer's lung), in mold-contaminated ventilation systems (humidifier lung), or in old homes seasonally contaminated by mold (summer-type pneumonitis).27,5 Mycobacterial antigens aerosolized by the mist that surrounds an operating hot tub can cause HP, colorfully described as hot-tub lung.
Commonly Described Causes of HP28
Open table in new window
Table
Exposure | Disease | Source of Antigen |
Avian | Bird fancier's lung, pigeon breeder's lung, poultry worker's lung | Feathers, droppings, serum proteins, intestinal mucins, avian immunoglobulin A |
Agriculture | Farmer's lung, Bagasse (sugar cane) lung, mushroom worker's lung, potato riddler's lung, paprika slicer's lung, wine maker's lung | Thermophilic actinomycetes, Aspergillus species, and other fungi in moldy hay or grains; moldy sugar cane; mushroom spores and thermophilic actinomycetes; moldy hay around potatoes, thermophilic actinomycetes, and others; Mucor stolonifer (on moldy paprika pods); B cinerea (noble rot on grapes) |
Water-based systems | Humidifier lung, hot-tub lung, sauna taker's lung, lifeguard's lung, sewage pneumonitis | Aerosolized molds, endotoxins, mycobacteria, thermophilic actinomycetes, Penicillium species, others |
Home environment | Summer-type pneumonitis, mold-contaminated walls, humidifiers, wallpaper | Trichosporon species, mold contamination in older and/or water-damaged homes
|
Chemicals | Chemical worker's lung, epoxy-resin lung, pyrethrum pneumonitis | Exposure to chemicals in manufacturing, laboratories, spray paints, heated epoxy resins, insecticides |
Exposure | Disease | Source of Antigen |
Avian | Bird fancier's lung, pigeon breeder's lung, poultry worker's lung | Feathers, droppings, serum proteins, intestinal mucins, avian immunoglobulin A |
Agriculture | Farmer's lung, Bagasse (sugar cane) lung, mushroom worker's lung, potato riddler's lung, paprika slicer's lung, wine maker's lung | Thermophilic actinomycetes, Aspergillus species, and other fungi in moldy hay or grains; moldy sugar cane; mushroom spores and thermophilic actinomycetes; moldy hay around potatoes, thermophilic actinomycetes, and others; Mucor stolonifer (on moldy paprika pods); B cinerea (noble rot on grapes) |
Water-based systems | Humidifier lung, hot-tub lung, sauna taker's lung, lifeguard's lung, sewage pneumonitis | Aerosolized molds, endotoxins, mycobacteria, thermophilic actinomycetes, Penicillium species, others |
Home environment | Summer-type pneumonitis, mold-contaminated walls, humidifiers, wallpaper | Trichosporon species, mold contamination in older and/or water-damaged homes
|
Chemicals | Chemical worker's lung, epoxy-resin lung, pyrethrum pneumonitis | Exposure to chemicals in manufacturing, laboratories, spray paints, heated epoxy resins, insecticides |
The most common type of HP in children is bird fancier's lung. Most often, the contact is with identified household pets, but, in many cases, the contact may be less obvious. HP has been reported after bird exposure from parental hobbies or occupations, including parental pigeon breeding,29 pheasant raising,30 and working on a turkey farm.31 Relevant exposures may be from nearby bird activity, with reported cases of HP resulting from birds congregating by a backyard pool,29 goose droppings tracked inside from a contaminated outdoor environment,32 wild city pigeons nesting just outside the home,33 birds nesting near the air intake of an air-conditioning system,34 and neighbors engaged in bird breeding.35 Live birds are not necessary to cause bird fancier's lung. Exposure to avian antigens from a feather duvet (feather duvet lung) has been linked to HP.36,37
Exposure to mold–contaminated moist organic material is a frequent cause of HP. Farmer's lung has been reported among children living on farms, especially in children exposed to moist or moldy hay or grains.38,39 Summer-type pneumonitis is classically described in the mid and southern parts of Japan, with onset during summer, resolution by mid-autumn, and recurrence the following summer. It is caused by fungal growth in older wooden homes stimulated by warm, moist summers.40,27 This summer-type pneumonitis has been described outside of Japan where similar conditions occur.41,42
Sources of mold in the child's environment may not be obvious. A compost heap in a play area caused HP in one child.43 HP was diagnosed in a child exposed to moldy hay at a horseback-riding school.44 A familial cluster of chronic HP was caused by mold that collected behind torn wallpaper and beneath worn carpets.45 Mold that contaminated a basement shower caused HP in several children.46
Wherever aerosolized water is present, HP can occur. Mold contamination of humidifiers has led to the disease in adults and children.47,48,49,50 Aerosolized endotoxin generated from a water spray in an indoor swimming pool has been implicated in lifeguard's lung.51 Hot-tub lung is believed to be a hypersensitivity reaction to contamination of hot-tub water by Mycobacterium avium intracellulare complex or mold in a hot tub.52,53
Finding the source of contaminated water may take some investigation. Hot-tub lung has been described in teenagers who used their family's or friend's hot tub.52 A central humidification system that nebulizes water into the heating system caused a cluster of HP cases in a family.47
Low molecular weight chemicals, such as isocyanates (eg, in spray paint and glue), phthalic anhydride (in epoxy resin), and pyrethrum (an insecticide), are thought to cause HP by combining with human proteins to form complete antigens.54
To diagnose HP, the key lies in a detailed history. The clinician has to maintain a high index of suspicion. Reaching the diagnosis can be difficult because symptoms are often nonspecific and the available diagnostic tests are imperfect. However, taking appropriate, effective action to eliminate the inciting exposure can prevent substantial pulmonary morbidity.
Diagnostic criteria proposed for adults are generally appropriate for children. Nonetheless, many of these criteria require invasive tests or radiation exposure, and some of the testing is difficult to perform in young children.
The diagnosis of HP is generally considered to be confirmed if at least 4 major criteria and 2 minor criteria are present and if alternative diagnoses are excluded. These diagnostic criteria may be summarized as follows:55
- Major diagnostic criteria
- Symptoms compatible with HP
- Evidence of exposure to an appropriate antigen apparent from the patient's history or from antibody detected in serum, BALF, or both
- Findings compatible with HP on chest radiography or high-resolution CT (HRCT) scanning
- Lymphocytosis observed in BALF
- Lung biopsy results that reveal histologic changes compatible with HP
- Positive finding from a natural challenge (ie, symptoms and laboratory abnormalities reproduced after exposure to the offending antigen
- Minor diagnostic criteria(almost always present but nonspecific)
- Bibasilar crackles
- Decreased capacity of the lung to diffuse carbon monoxide
- Hypoxemia whether patient is at rest or exercising
More on Hypersensitivity Pneumonitis |
 Overview: Hypersensitivity Pneumonitis |
| Differential Diagnoses & Workup: Hypersensitivity Pneumonitis |
| Treatment & Medication: Hypersensitivity Pneumonitis |
| Follow-up: Hypersensitivity Pneumonitis |
| Multimedia: Hypersensitivity Pneumonitis |
| References |
| Further Reading |
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Keywords
Hypersensitivity pneumonitis, HP, extrinsic allergic alveolitis, EAA, bird fancier's lung, pigeon fancier’s lung, bird breeder's lung, pigeon breeder's lung, farmer's lung, recurrent pneumonitis, pulmonary fibrosis, emphysema, hypersensitivity pneumonitides, farm worker's lung, thermophilic actinomycetes, winemaker's lung, Botrytis cinerea, coffee worker's lung, coffee bean dust, lifeguard's lung
aerosolized endotoxin, poultry worker's lung, avian antigens, laboratory worker's lung, rodent antigens, miller's lung, wheat weevil, woodworker's lung, Bacillus subtilis, epoxy-resin lung, Phthalic anhydride, spontaneous pneumothorax, end-stage lung disease, acute respiratory symptoms, pneumonia, digital clubbing, chronic cough, dyspnea, cyanosis, bird fancier's lung, pigeon breeder's lung, Aspergillus species, moldy hay, Mucor stolonifer, humidifier lung, hot-tub lung, sauna taker's lung, sewage pneumonitis, summer-type pneumonitis, Trichosporon species
